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Blood Bank > Genes, Antigens, Antibodies, and Basic Testing > Flashcards

Genes, Antigens, Antibodies, and Basic Testing Flashcards

1
Q

Leucocyte Poor Red Cells

A

Used primarily for patients with repeated febrile non hemolytic (FNH) reactions or those that are chronically transfused

Usually due to the presence of cytokines released from white cells or alloimmunization to HLA or leukocyte antigens

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2
Q

Differentiating A1 and A2

A

Based on reactivity differences with anti-A1, lectin from Dolichos biflorus, which agglutinates A1 but NOT A2 cells

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3
Q

Anti-H Differentiation

A

Lectin from Ulex europaeus, which will agglutinate O cells (HH or Hh), but not Bombay cells (hh)

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4
Q

Se gene

A

Two alleles, Se (secretors) and se

Allow expression of ABO and H (A, B, H, and Le^b) antigens in body fluids

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5
Q

Combination of H and Le genes

A

H and Lea will be on red cells, only Lea only in saliva

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6
Q

Combination of H, Se, and Le genes

A

H and Leb on the red blood cells, H, Leb, and Lea in small amounts in body fluids

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7
Q

Rh null

A

No D, C, E, c, or e antigens on cells, associated with hemolytic anemia as these structures are associated with RBC membrane integrity

Inheritance of 2 nonfunctional RHCE alleles with deletion of both RHD alleles

OR homozygous recessive inheritance of the regulator RHAG with normal RHCE and RHD

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8
Q

Deleted cells (D–)

A

Missing some or more of the normal Rh alleles

Doesn’t react with anti-E, anti-e, anti-C, or anti-c

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9
Q

Rh antibodies

A

Typically RBC stimulated

Pregnancy (cause hemolytic disease of the newborn as they cross the placenta)

Transfusions (will cause transfusion reactions)

IgG, do not activate complement, will not agglutinate saline suspended RBCs unless IAT is used

C/e and E/c are usually together

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10
Q

Lewis Antigen Creation

A

Includes plasma antigens that absorb onto RBCs

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11
Q

Lewis antibodies

A

IgM, usually only in Le(a-b-) patients, can be temporarily seen during pregnancy

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12
Q

Landsteiner’s Rule

A

If an individual has the antigen, they will not have the antibody

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13
Q

ABO Expression/makeup

A

Can be secreted if the proper genes are present, glycolipids or glycoproteins, develop into full expression between 2-4 years of age

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14
Q

H antigen

A

H gene contains the alleles H and h, it is the building block for A and B antigens

Antigen is a sugar acceptor, with A and B accepting different sugars and O accepting none

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15
Q

Anti-A and anti-B

A

IgM and therefore able to activate complement, causing agglutination

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16
Q

Problems with Forward Typing

A

(Extra antigen, weak antigens)

  • ABO subgroups
  • Acquired B phenotype
  • Bone marrow/stem cell transplants
  • Polyagglutination
  • Rouleaux
  • Transfusion of non-specific blood
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17
Q

Problems with Reverse Typing

A

(unexpected antibodies or weak/missing antibodies)

  • A subgroups with Anti-A1
  • Cold alloantibodies
  • Elderly
  • Newborns
  • Rouleaux
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18
Q

Bombay Phenotype

A

Types as an O, with alloanti-H that can activate complement and cause hemolysis

Can transmit functional A and B genes to their children, even though they can’t produce them themselves

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19
Q

Rh Genes

A

Controlled by RHD (D expression) and RHCE (C, c, E, e)

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20
Q

Fisher-Race Terminology

A

Rh antigens, D, C, c, E, e, Cw, G,…

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21
Q

Wiener Terminology

A

Rh haplotype terminology, R1, R2 for CDe/CDe

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22
Q

Weak D

A

Weak D testing is carried out on any cell that previously gave a negative reaction with anti-D and Rh control

Caused by weaker expression of the cDe haplotype, from the C antigen is inherited trans to the D antigen

Can be transfused with D-Neg blood

23
Q

Partial D

A

Lacking 1 or more epitopes of D antigen, and makes antibody for missing parts

Type as D Pos, create Ab after transfusion or pregnancy

24
Q

F/ce antigen

A

Expressed when c and e are on the same haplotype

25
Q

Ce/rhi antigen

A

Expressed when C and e are on the same haplotype, D-Pos patients who make anti-C

26
Q

Cw antigen

A

Low frequency antigen

27
Q

V/ces antigen

A

30% prevalence in African Americans

28
Q

G antigen

A

Appears anti-D and anti-C

29
Q

DAT

A

Use AHG (antihuman globulin) to detect IgG and complement, which indicates the possibility of immune mediated hemolysis in the patient, done for:

  • autoimmune hemolytic anemia
  • HDN (hemolytic disease of newborn)
  • Drug-related mechanism
  • Transfusion reaction
30
Q

Antibody Screen

A

For patients needing transfusions, pregnancies, donors and those having transfusion reactions; uses O donor cells with known antigens

31
Q

Hemolytic Disease of the Newborn

A

D- mothers makes antibodies to D+ baby in first pregnancy, newborns show positive DAT, increased serum bilirubin

32
Q

2 - 5% Washed Red Cell Suspension

A

Visibility of antigen and antibody complexes is dependent on the number of antigen sites available

33
Q

Grading Reactions with Anti-A and Anti-B

A

Anti-A and anti-B are saline- reactive antibodies, saline reactive antibodies are most often of the IgM class and react strongly at room temperature, and strongest at 40 C.

34
Q

Antiglobulin Test

A

DAT

  • Detects in-vivo sensitization of IgG alloantibodies
  • IgG autoantibodies
  • Complement components

(IAT is in-vitro)

35
Q

For antiglobulin tests, why do you Incubate RBCs with antisera?

A

Allows time for antibody molecule attachment to RBC antigen

36
Q

For antiglobulin tests, why do you Centrifuge?

A

Accelerates agglutination by bringing cells closer together

37
Q

Albumin Reaction Media

A

Allows sensitized cells to come close together to form agglutination lattices

38
Q

PeG Reaction Media

A

Concentrates Ab and creates a low-ionic sln that allows greater Ab uptake

39
Q

ABO gene locus

A

C’some 9

40
Q

Antigen Development

A

A and B develop 5th week fetal life, but increase slowly, formed from complex interaction of H/h and ABO genes

41
Q

Type 1 Precursor Chain

A

Glycoprotein precursor of ABH Ag

42
Q

Type 2 Precursor Chain

A

Glycolipid precursor of ABH Ag on RBC surface

43
Q

ABO Ab

A
  • Usually IgM, can be IgG/IgA in small quantities
  • React best at RT
  • Activate complement (including the IgG at RT)
  • Saline agglutinins
44
Q

Anti-A,B

A

IgG form is found in serum from sensitized O Pts (i.e. O mothers carrying A or B fetuses), which can cause HDFN

45
Q

Anti-H

A

A weak, cold reacting Ab in A1, A1B people

46
Q

Anti-A1

A

Non-recative a Body Temp so Clinically Insignificant, if it is reactive at that temp, it can cause in vivo RBC destruction and is clinically significant

47
Q

Weak/Missing Ab

A

Most frequent cause of ABO discrepancy

Low ABH Ab titers are found in the young, sick or debilitated and will not be picked up by routine testing, corrected by optimizing the reverse reaction conditions such as lower temp. (A/C and O cells should be controls)

48
Q

Weak/Missing Ag

A

A/B subgroups, or weakening Ag strength in conditions like Leukemia

49
Q

Acquired B Phenotype

A

Can be caused by intestinal obstruction, carcinoma in colon/rectum, any gastrointestinal disorder that obstructs or slows movement, allowing intestinal bacteria into bloodstream

50
Q

Weak D Genetics

A

Caused by many different changes in the RHD gene, Types 1, 2, and 3 are 90% of the cases found in Europeans

51
Q

Compound Ags

A

Are directed to the shared epitopes of C/c or E/e on the same protein

52
Q

Immunogenicity of Rh Ag

A

D is most immunogenic, e is the least

53
Q

Rh Testing

A

Use antisera that has been chemically modified with a sulflhydryl compound that weakens the disulfide bonds at the hinge region and allows the IgG to flex

Blood Bank (11 decks)

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